Saudi Journal of Kidney Diseases and Transplantation

: 2017  |  Volume : 28  |  Issue : 6  |  Page : 1412--1415

Acute kidney injury: A rare complication of mothball (Naphthalene) poisoning

Sudha Ekambaram, KM Chandan Kumar, Vijayakumar Mahalingam 
 Department of Pediatric Nephrology, Mehta Children’s Hospital, Chennai, Tamil Nadu, India

Correspondence Address:
Sudha Ekambaram
Department of Pediatric Nephrology, Mehta Children’s Hospital, Chennai, Tamil Nadu


Naphthalene poisoning is an uncommon poisoning due to its pungent smell, taste, insolubility in water, and poor absorption from the gut. It rarely occurs in suicidal attempts in adults and in accidental ingestion by children. We present a diagnostic and therapeutic challenge encountered while treating a child with naphthalene-induced acute severe hemolytic anemia and acute kidney injury from accidental ingestion.

How to cite this article:
Ekambaram S, Chandan Kumar K M, Mahalingam V. Acute kidney injury: A rare complication of mothball (Naphthalene) poisoning.Saudi J Kidney Dis Transpl 2017;28:1412-1415

How to cite this URL:
Ekambaram S, Chandan Kumar K M, Mahalingam V. Acute kidney injury: A rare complication of mothball (Naphthalene) poisoning. Saudi J Kidney Dis Transpl [serial online] 2017 [cited 2023 Feb 4 ];28:1412-1415
Available from:

Full Text


Naphthalene poisoning is an uncommon poisoning due to its pungent smell, taste, insolubility in water, and poor absorption from the gut. It rarely occurs in suicidal attempts in adults and in accidental ingestion by children. Rare cases of mothball abuse predominantly by inhalation do occur.[1] Among 22 children aged less than 15 years admitted for poisoning, 4% were due to naphthalene poisoning.[2] The most common age group was 0–5 years constituting 81.2% of total patients of poisonings, followed by 5–10 years (16.1%). There was an overall male predominance, with male-to-female ratio of 1.6:1.[3] Another factor that may increase the risk of accidental pediatric exposures to mothballs is the small size and presence of coloring, which may attract attention from toddlers and children.[4] Most of the poisoning with mothballs seem to occur in the developing countries.[5],[6],[7] We present a diagnostic and therapeutic challenge encountered while treating a child with naphthaleneinduced severe hemolytic anemia and acute kidney injury (AKI) from accidental ingestion.

 Case Report

A two-year-old developmentally normal toddler boy was referred to our center with concern of rising renal parameters. He had fever of two days’ duration which was associated with reduced urine output, cola-colored urine, and yellowish discoloration of eyes, noted on day one of fever. Preliminary investigations revealed blood hemoglobin of 5.5 g/dL, total leukocyte count of 21,000/mm3, platelet count of 400,000/mm3, and corrected reticulocyte count of 1.7, and direct Coombs test was negative. Blood urea was 124 mg/dL, serum creatinine was 1.8 mg/dL, lactate dehydrogenase (LDH) was 5700 U/L (120–300 U/L), serum bilirubin was 3.9 mg/dL with indirect fraction of 2.1 mg/dL, serum glutamicoxaloacetic transaminase was 62 U/L, and serum glutamic-pyruvic transaminase was 108 U/L. Urine protein showed 1+ by dipstick with 8–10 red blood cells per high-power field (RBC/HPF), and urine was negative for hemoglobin and myoglobin. Hemolytic-uremic syndrome (HUS) with a normal platelet count was one of the possible diagnoses.[8] In the next two days, the child continued to be febrile, icteric, pale looking, normotensive, and non-edematous, but the serum creatinine progressively increased. The possibility of malaria or leptospiral infection was considered and eliminated. Further evaluation showed hemoglobin of 5.9 g/dL, total white blood cell count of 26,000/mm3, platelet count of 260000/mm3, serum creatinine of 6.1 mg/dL, serum LDH of 2464 U/L, and serum glucose-6-phosphate dehydrogenase (G6PD) of 9.3 U/gHb (6.4–18.7 U/gHb); peripheral smear showed hypochromic, microcytic anemia, anisopoikilocytosis, spherocytes, and polychromasia with adequate platelets, suggestive of hemolysis and urinalysis showed proteinuria 2+ by dipstick with 8–10 RBC/HPF. Liver function tests and coagulation profile were normal, and ultrasonography (USG) of the abdomen showed structurally normal kidneys. As the cause remained uncertain, on further probing, the mother informed about the possibility of ingestion of mothballs by the child two days before the onset of symptoms. No medical attention was sought as the child was apparently normal. The child was started on hemodialysis (HD) in view of AKI with estimated glomerular filtration rate (eGFR) of 6.17 mL/ min/1.73 m2 along with other supportive measures. He was transfused packed red blood cells for anemia. The child developed transient hypertension which was treated with calcium channel blockers. As the history of mothball ingestion was doubtful and cause of AKI was not apparent despite extensive investigations, renal biopsy was performed on day 5 of admission, which revealed acute tubular injury with pigment casts [Figure 1]. After a cumulative 9 h of HD, it was discontinued with the serum creatinine being 1.4 mg/dL. The child was discharged with serum creatinine of 0.8 mg/dL, hemoglobin of 9.3 g/dL, LDH of 229 U/dL, serum bilirubin of 0.4 mg/dL, G6PD of 5.6 U/L, a normal peripheral smear with trace proteinuria. On follow-up two months later, he had normal renal, hepatic, and hematological parameters.{Figure 1}


Naphthalene and 1, 4-dichlorobenzene are the major ingredients in mothballs. It is a common household pesticide used to protect clothes from moths (Tineola bisselliella and Tinea pellionella). It sublimates and the fume has insecticidal properties. One mothball can contain 0.5–5 g of naphthalene.[9] The fatal dose for naphthalene in humans is unknown, but as little as one mothball can result in toxicity in children. Deaths have been reported the following ingestion of naphthalene balls.[10],[11] Naphthalene is erratically absorbed when ingested in the pediatric population. Other routes of exposure include inhalational and skin contact. It is rapidly absorbed when inhaled. Dermal absorption in humans, especially in infants, maybe significant and further enhanced by prior application of oils.[12] Most countries have replaced naphthalene with 1, 4-dichlorobenzene and mothballs have been banned. In resourcelimited countries, these products are still used, are poorly labeled, and consumers are often not aware of their contents.[13]

The rapid onset of hemolytic anemia, mild icterus, and AKI with preceding fever was suggestive of atypical HUS (aHUS). The absence of the third component of aHUS, thrombocytopenia, and absence of thrombotic microangiopathy on renal biopsy ruled out the condition. Being in a malarial endemic area, this case could have been mistaken for malaria if the history of exposure to mothballs was not obtained. Similar observation was reported by Nte et al.[14] The clinical consequences of mothball poisoning may include headache, vomiting, diarrhea, abdominal pain, fever, and altered mental status.[12] The most significant toxicity of naphthalene is hematologic. Hemolytic anemia leading to hematuria and methemoglobinemia can occur.[15]

Acute exposure can result in severe hemolysis in individuals who have mild low or even normal G6PD levels, similar to the index child who had mild enzyme deficiency.[16] During the acute phase of hemolysis, individuals with mild enzyme deficiency may have normal enzyme activity levels due to increased release of young red blood cells with normal enzyme activity.[13],[17] Hemolysis occurs particularly in patients with G6PD deficiency because they have a low tolerance to oxidative stress. There are various mechanisms within the RBCs, which prevent toxicity from oxidative stress. The most important protective effect is through the generation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) from the hexose monophosphate shunt. The NADPH is used to maintain adequate stores of reduced glutathione to prevent hemolysis from oxidative stress. Individuals who have G6PD do not produce as much NADPH. Such individuals have lower levels of glutathione and are subsequently at much higher risk of hemolysis and methemoglobinemia after exposure to naphthalene.[18]

Renal failure as a complication of naphthaleneinduced hemolysis and hemoglobinuria has been reported.[19] Mechanical trauma to erythrocytes liberates hemoglobin into plasma, which is filtered in the glomerulus and is incorporated into proximal tubules through the megalincubulin receptor system present on the apical surface of these cells; intracellular hemoglobin then dissociates into heme and globin. The increased intracellular level of heme is potentially cytotoxic and can cause AKI through three main mechanisms: decreased renal perfusion, direct cytotoxicity, and intratubular casts formed from the interaction of heme proteins with Tamm–Horsfall protein. Cytotoxic effects of large amounts of heme result from its lipophilic, oxidant, pro-inflammatory, and apoptotic effects, and the mitochondria are particularly vulnerable to hememediated damage.[20]

Hemolysis can be slowly progressive and even delayed, as observed in the index child, who presented four days after ingestion. Hence, there is tendency to overlook the relationship with exposure. Similar observations have been reported by others.[7],[14],[21] He had remarkable improvement and was discharged on the day 12. There is no specific treatment for naphthalene poisoning. The management is symptomatic with packed red cell transfusions and monitoring of fluid and electrolyte balance. Alkalis have been recommended in the presence of hemoglobinuria to prevent its deposition in renal tubules. Administration of milk, fats, and oils should be avoided as they may enhance absorption of naphthalene.

Although there have been previous reported cases of mothball poisoning causing hemolysis, there are no reported cases of AKI in children from India. Case studies are concerned with adults.[22] The aim of this index case is not only to report an unusual presentation but also to draw the attention of clinicians and regulatory agencies to the hazard associated with unregulated use of this chemical.[23] It is more so as exposure to mothballs is often forgotten when evaluating children for sudden unexplained onset of hemolytic anemia and AKI.


A two-year toddler presenting with acute hemolysis and AKI can entertain a number of possibilities. The value of careful history elicitation which primarily benefitted in the right diagnosis and good outcome is highlighted.

Conflict of interest: None declared.


1Weintraub E, Gandhi D, Robinson C. Medical complications due to mothball abuse. South Med J 2000;93:427-9.
2Asghar A, Anees M, Mahmood KT. Accidental poisoning in children. J Biomed Sci Res 2010; 2:284-9.
3Khadgawat R, Garg P, Bansal P, Arya A, Choudhary B. Accidental poisoning. Indian Pediatr 1994;31:1555-7.
4Lim HC. Mothballs: Bringing safety issues out from the closet. Singapore Med J 2006;47: 1003.
5Rahman MM, Mogni Mowla SG, Rahim A, et al. Severe haemolytic anaemia due to ingestion of naphthalene (mothball) containing coconut oil. J Coll Physicians Surg Pak 2012;22:740-1.
6Santhanakrishnan BR, Ranganathan G, Raju VB. Naphthalene induced haemolytic anaemia with haemoglobinuria. Indian J Pediatr 1973;40:195-7.
7Annamalai KC, Shrikiran A, Mundkur SC, Chaitanya Varma PV. Acute naphthalene toxicity presenting with metabolic acidosis: A rare complication. J Acute Dis 2012;1:75-6.
8Sallée M, Ismail K, Fakhouri F, et al. Thrombocytopenia is not mandatory to diagnose haemolytic and uremic syndrome. BMC Nephrol 2013;14:3.
9Naphthalene. Available from: https://www.en. [Last accessed on 2014 Aug 10].
10Gupta R, Singhal PC, Muthusethupathy MA, Malik AK, Chugh KS. Cerebral oedema and renal failure following naphthalene poisoning. J Assoc Physicians India 1979;27:347-8.
11Kurz JM. Naphthalene poisoning: Critical care nursing techniques. Dimens Crit Care Nurs 1987;6:264-70.
12Kuffner EK. Camphor and moth repellants. In: Goldfrank LR, Flomenbaum NE, Lewin NA, et al, eds. Goldfrank’s Toxicologic Emergencies. 7th ed. New York: McGraw-Hill; 2002. p. 1295-302.
13Aliyu I, Ibrahim ZF. Haemolytic anemia and mothball toxicity: A case report. Int Med J Sifa Univ 2014;1:39-41.
14Nte A, Anochie I, Eke F. Naphthalene poisoning in children: A report of two cases. Niger J Pediatr 2006;33:60-3.
15Kapoor R, Suresh P, Barki S, Mishra M, Garg MK. Acute intravascular hemolysis and methemoglobinemia following naphthalene ball poisoning. Indian J Hematol Blood Transfus 2014;30:317-9.
16Valaes T, Doxiadis SA, Fessas P. Acute hemolysis due to naphthalene inhalation. J Pediatr 1963;63:904-15.
17Beutler E. Glucose-6-phosphate dehydrogenase deficiency. N Engl J Med 1991;324:169-74.
18Todisco V, Lamour J, Finberg L. Hemolysis from exposure to naphthalene mothballs. N Engl J Med 1991;325:1660-1.
19Chugh KS, Singhal PC, Sharma BK, et al. Acute renal failure due to intravascular hemolysis in the North Indian patients. Am J Med Sci 1977;274:139-46.
20Qian Q, Nath KA, Wu Y, Daoud TM, Sethi S. Hemolysis and acute kidney failure. Am J Kidney Dis 2010;56:780-4.
21Lim HC, Poulose V, Tan HH. Acute naphthalene poisoning following the nonaccidental ingestion of mothballs. Singapore Med J 2009;50:e298-301.
22Kundra TS, Bhutatani V, Gupta R, Kaur P. Naphthalene poisoning following ingestion of mothballs: A Case report. J Clin Diagn Res 2015;9:UD01-2.
23Sudakin DL, Stone DL, Power L. Naphthalene mothballs: Emerging and recurring issues and their relevance to environmental health. Curr Top Toxicol 2011;7:13-9.